ReviewJournal of Parkinson's disease2022
Role of NLRP3 Inflammasome in Parkinson's Disease and Therapeutic Considerations.
Review in Journal of Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 68 citations in OpenAlex.
- From neuroinflammation to immune reprogramming: Nanozyme-Integrated nanoplatforms for neuroimmune modulation in Parkinson's disease.Materials today. Bio · 2026Article
- Trans-Vitisin B Targets Neuroinflammation, Oxidative Stress, and Tau Pathology to Improve Behavioral Outcomes in a Mouse Model of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- The mitophagy-inflammasome axis: a shared pathological hub in Alzheimer's and Parkinson's diseases.Translational neurodegeneration · 2026Review
- Comparative Peripheral Blood Transcriptomic Profiles in Parkinson's Disease and Restless Legs Syndrome: An Exploratory Between-Cohort Analysis.International journal of molecular sciences · 2026Article
- Intranasal 6-OHDA Induces TRPM3-mediated Neuroinflammation in the pVTA: A Preclinical Early-stage Parkinson's Disease Model.Molecular neurobiology · 2026Article
- Deconstructing the Master Switch: Advances in Direct NLRP3 Inhibition.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Cannabidiol Protects Against 1-Methyl-4-Phenylpyridinium and Manganese-Induced Neurotoxicity via Nod-Like Receptor Protein 3 Inflammasome Suppression.Journal of biochemical and molecular toxicology · 2026Article
- Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026Review
- ATP13A2 restrains macrophage NLRP3 inflammasome activation to repress neurodegeneration via modulating mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.Current issues in molecular biology · 2026Review
- Sources of Oxidative Stress in Parkinson's Disease: Pathways and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Do microplastics play a role in the pathogenesis of neurodegenerative diseases? Shared pathophysiological pathways for Alzheimer's and Parkinson's disease.Molecular and cellular biochemistry · 2026Review
- Mitophagy-NLRP3 Inflammasome Crosstalk in Parkinson's Disease: Pathogenic Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Organosulfur Compounds: Potential Therapeutics for Parkinson's Disease.CNS & neurological disorders drug targets · 2026Review
- Micro- and nanoplastics as environmental modifiers of neuroimmune dysfunction in Parkinson's disease.Frontiers in neuroscience · 2026Review
- Differential Peripheral NLRP3 Inflammasome Expression in Patients With Parkinson's Disease and Patients With Multiple System Atrophy.Journal of movement disorders · 2026Article
- Parkinson's disease-associated alterations in DNA methylation and hydroxymethylation in human brain.NPJ Parkinson's disease · 2025Article
- Mechanistic Characterization of a Small Molecule as a Direct NLRP3 Inhibitor via Binding to the NACHT Domain.Journal of medicinal chemistry · 2025Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disease, with two main pathological features: misfolded α-synuclein protein accumulation and neurodegeneration. Inflammation has recently been identified as a contributor to a cascade of events that may aggravate PD pathology. Inflammasomes, a group of intracellular protein complexes, play an important role in innate immune responses to various diseases, including infection. In PD research, accumulating evidence suggests that α-synuclein aggregations may activate inflammasomes, particularly the nucleotide-binding oligomerization domain-leucine-rich repeat-pyrin domain-containing 3 (NLRP3) type, which exacerbates inflammation in the central nervous system by secreting proinflammatory cytokines like interleukin (IL)-18 and IL-1β. Afterward, activated NLRP3 triggers local microglia and astrocytes to release additional IL-1β. In turn, the activated inflammatory process may contribute to additional α-synuclein aggregation and cell loss. This review summarizes current research evidence on how the NLRP3 inflammasome contributes to PD pathogenesis, as well as potential therapeutic strategies targeting the NLRP3 inflammasome in PD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.